Neuroendocrine activation after myocardial infarction

Remes, Jouko

doi:10.1136/hrt.72.3_suppl.s65

Cited by 22 publications

(16 citation statements)

References 25 publications

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“…ANP and BNP are produced in the myocardial cells of the atrium and ventricle, respectively, and are secreted in response to distention of the cardiac chambers and/or arterial pressure elevation. These peptides play a central role in modulating extracellular volume homeostasis and blood pressure by counteracting the actions of SNS and RAAS (144,169,219). Plasma levels of ANP and BNP are increased in patients with HF and positively correlate with the degree of left ventricular dysfunction (25,38,156,169,204,228).…”

Section: Upregulation Of Nhe3 Transport Activity In Heart Failure Maymentioning

confidence: 98%

Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction

Girardi

Sole

2012

American Journal of Physiology-Cell Physiology

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The Na(+)/H(+) exchanger-3 (NHE3) belongs to the mammalian NHE protein family and catalyzes the electro-neutral exchange of extracellular sodium for intracellular proton across cellular membranes. Its transport function is of essential importance for the maintenance of the body's salt and water homeostasis as well as acid-base balance. Indeed, NHE3 activity is finely regulated by a variety of stimuli, both acutely and chronically, and its transport function is fundamental for a multiplicity of severe and world-wide infection-pathological conditions. This review aims to provide a concise overview of NHE3 physiology and discusses the role of NHE3 in clinical conditions of prominent importance, specifically in hypertension, diabetic nephropathy, heart failure, acute kidney injury, and diarrhea. Study of NHE3 function in models of these diseases has contributed to the deciphering of mechanisms that control the delicate ion balance disrupted in these disorders. The majority of the findings indicate that NHE3 transport function is activated before the onset of hypertension and inhibited thereafter; NHE3 transport function is also upregulated in diabetic nephropathy and heart failure, while it is reported to be downregulated in acute kidney injury and in diarrhea. The molecular mechanisms activated during these pathological conditions to regulate NHE3 transport function are examined with the aim of linking NHE3 dysfunction to the analyzed clinical disorders.

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Section: Upregulation Of Nhe3 Transport Activity In Heart Failure Maymentioning

confidence: 98%

Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction

Girardi

Sole

2012

American Journal of Physiology-Cell Physiology

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“…The relationship between elevated natriuretic peptide levels and survival is believed to result mainly in their reflection of increased LV filling pressure secondary to LV dysfunction (11). In patients with AMI, plasma NT-pro BNP measured 48 to 120 hours after the index event has been shown to correspond with LV function and long-term survival (12,13).…”

Section: Introductionmentioning

confidence: 98%

Relative Role of NT-pro BNP and Cardiac Troponin T at 96 hours for Estimation of Infarct Size and Left Ventricular Function After Acute Myocardial Infarction

Steen¹,

Futterer²,

Merten³

et al. 2007

J. of Cardiovascular Magnetic Resonance

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“…In the acute phase of a myocardial infarction plasma renin activity and plasma levels of norepinephrine, atrial natriuretic peptide, endothelin and arginine vasopressin increase in most patients [1][2][3][4][5] . Until recently, this neurohumoral activation was considered to have disappeared by 7 to 10 days, except for persistent elevation of atrial natriuretic peptide in patients with systolic left ventricular dysfunction and persistent activation of plasma renin activity in patients with heart failure or using diuretic drugs [1] .…”

Section: Introductionmentioning

confidence: 99%

“…The degree of neurohumoral activation both during the first days of myocardial infarction in unselected populations of patients [3][4][5][6][7][8] , and at the time of hospital discharge in patients with asymptomatic left ventricular dysfunction [9,10] has incremental prognostic value. One would expect that persistent or new neurohumoral activation after hospital discharge in the latter group signifies a worse prognosis, but to our knowledge there is no direct evidence to support this.…”

Section: Introductionmentioning

confidence: 99%

“…Alternatively, patients with early post-infarction asymptomatic left ventricular dysfunction could go one of two ways: maintain a state of more neurohumoral activation and evolve into patients with symptomatic left ventricular dysfunction, such as those of the SOLVD treatment group [11] , or reduce neurohumoral activation and evolve as patients such as the SOLVD prevention group [11] . Finally, although neurohumoral activation has prognostic significance in patients with left ventricular dysfunction early post-infarction [3][4][5][6][7][8][9][10] and in patients with chronic left ventricular dysfunction [11][12][13][14][15] , differences in the relative importance of the various neurohormones exists. This suggests that early activation of some neurohormones is more frequently reduced during the first 3 months post-infarction and that these neurohormones may contribute to early remodelling and prognosis rather than to long-term prognosis.…”

Section: Introductionmentioning

confidence: 99%

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Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

Vantrimpont

Rouleau

Ciampi

et al. 1998

European Heart Journal

103

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Aims To describe the temporal evolution of neurohumoral activation in survivors of myocardial infarction with left ventricular dysfunction who are initially asymptomatic and to relate this to prognosis. Methods and ResultsPatients in the neurohumoral substudy (n=534) of the Survival and Ventricular Enlargement (SAVE) study had their neurohormones measured at baseline, 3, 12 and 24 months post-infarction, were followed 38 7 months and had these values related to prognosis. All patients had a left ventricular ejection fraction c40% early post-infarction. Atrial natriuretic peptide, aldosterone, norepinephrine and plasma renin activity decreased progressively over time. Patients with events had a persistent increase in these neurohormones with those dying within the first 24 months of follow-up having the greatest increase. Treatment with captopril affected only plasma renin activity (increase) and aldosterone (decrease). For patients who remained asymptomatic for the first 3 months postinfarction (n=471), by multivariate analyses (all neurohormones together with non-neurohumoral risk factors), 3-month plasma atrial natriuretic peptide and aldosterone were the most closely related to the development of severe heart failure or to the combined end-points (cardiovascular death, myocardial infarction, or severe heart failure). No neurohormone was related to recurrent myocardial infarction or to cardiovascular mortality. When the last neurohormone measured prior to an event was considered along with non-neurohumoral risk factors (adjusted univariate), atrial natriuretic peptide, aldosterone, norepinephrine and epinephrine were associated with prognosis indicating that a time-dependent analysis identified a closer relationship between neurohormones and events than that identified by 3-month values. However, by multivariate analyses atrial natriuretic peptide was the only neurohormone associated with an event, being associated with the development of severe heart failure (P<0·001) and the combined end-points (P=0·022). However, when neurohormones were considered as binary variables, activated or non-activated (defined as >1·96 SD above the mean of age-matched controls), an association between activation of norepinephrine prior to recurrent myocardial infarction (P<0·001) and combined end-points (P<0·01) and between activation of aldosterone and severe heart failure (P<0·05) was identified.Conclusions Neurohumoral activation decreases progressively post-infarction, but only in patients with a good prognosis. In patients with a left ventricular ejection fraction c40% and asymptomatic post-infarction plasma atrial natriuretic peptide at 3 months, aldosterone levels appeared to be the neurohormones most closely associated with prognosis. Increased levels of atrial natriuretic peptide, aldosterone and norepinephrine appear to be temporally most closely associated with events.

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Neuroendocrine activation after myocardial infarction

Cited by 22 publications

References 25 publications

Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction

Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction

Relative Role of NT-pro BNP and Cardiac Troponin T at 96 hours for Estimation of Infarct Size and Left Ventricular Function After Acute Myocardial Infarction

Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

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Neuroendocrine activation after myocardial infarction

Cited by 22 publications

References 25 publications

Deciphering the mechanisms of the Na+/H+ exchanger-3 regulation in organ dysfunction

Deciphering the mechanisms of the Na+/H+ exchanger-3 regulation in organ dysfunction

Relative Role of NT-pro BNP and Cardiac Troponin T at 96 hours for Estimation of Infarct Size and Left Ventricular Function After Acute Myocardial Infarction

Two-year time course and significance of neurohumoral activation in the Survival and Ventricular Enlargement (SAVE) Study

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Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction

Deciphering the mechanisms of the Na⁺/H⁺ exchanger-3 regulation in organ dysfunction